Genetically engineered T cells expressing a chimeric antigen receptor targeting malignant B cells; infused 2–10×10^6/kg within 7 days post-ASCT.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that recognizes B‑cell tumor antigens (e.g., CD19) independently of HLA, providing CD3ζ plus co‑stimulatory signaling (e.g., CD28 or 4‑1BB) to activate and expand the cells, leading to cytokine release and perforin/granzyme‑mediated cytotoxic killing of malignant B cells.
CD19-directed CAR-T cells bind CD19 on target cells and kill them via perforin/granzyme-mediated cytotoxicity.
Antibody–drug conjugate (ADC) also known as izalontamab brengitecan (iza-bren; BMS-986507); administered intravenously. The monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death.
The ADC binds EGFR on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload that induces DNA damage leading to cell death.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills them via complement-dependent cytotoxicity (CDC), Fc-mediated effector functions (ADCC/ADCP), and induction of apoptosis.
Antibody–drug conjugate (ADC) also known as izalontamab brengitecan (iza-bren; BMS-986507); administered intravenously. The monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death.
ADC binds HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload that inhibits topoisomerase I, causing DNA damage and tumor cell death.
MC1R-targeted peptide radiopharmaceutical delivering alpha-particle therapy via 212Pb decay (212Pb→212Bi/212Po) to induce short-range, high-LET DNA double-strand breaks in melanoma cells; administered IV approximately every 8 weeks as mono- or combination therapy.
MC1R-targeted peptide (VMT01) delivers the alpha-emitting radionuclide 212Pb (decaying via 212Bi/212Po) to MC1R-expressing tumor cells, producing short-range, high-LET alpha radiation that induces clustered DNA double-strand breaks and tumor cell death.
The VMT01 peptide binds MC1R on tumor cells and delivers 212Pb; subsequent alpha-particle emissions (via 212Bi/212Po) deposit short-range, high-LET radiation that induces clustered DNA double-strand breaks, leading to tumor cell death.